Genes beginning with "h"

Obtained as a suppressor of the colonial growth and low cAMP level of cr-1.
High aerial hyphae are
formed on agar medium. The double mutant cr-1; hah conidiates, but the single hah
mutant does not
(1399, 1404). See also ref. (1020).

Lacks
the salicylhydroxamic acid (SHAM)-sensitive respiratory pathway. Cannot produce the
hydroxamate-sensitive respiratory pathway when grown in the presence of chloramphenicol.
Grows
slowly in the presence of antimycin A (595). The double mutant has; azs is unable to grow in the
presence of antimycin A, whereas wild type and has+; azs grow well. The
has; azs strain (called ANT-1:
antimycin-sensitive) was used to obtain mutants resistant to oligomycin (596) and mutants deficient in
succinate dehydrogenase (590).

Used
for the strain am1ad-3B cyh-1 (FGSC No. 4564), which is able to form
vigorous wild-type
heterokaryons with OR-compatible mutant strains of either mating type (1564). Because mat a allele am1
is inactive, the helper-1 component of such a heterokaryon is a passive partner when the
heterokaryon is
used as parent in a cross. Only nuclei of the active partner participate in karyogamy, meiosis, and
the
production of sexual progeny. The helper-1 strain has proved useful for
crossing otherwise infertile or
poorly fertile strains (1565), for rescuing and sheltering inviable or unstable genotypes (114, 1576), and
for determining whether strains of undetermined mating type are
OR-heterokaryon-compatible.

Used
for the strain am1ad-3B cyh-1 (FGSC No. 4564), which is able to form
vigorous wild-type
heterokaryons with OR-compatible mutant strains of either mating type

If two
strains carry different alleles at one or more het loci, they are unable to form stable
heterokaryons
(715, 716). Incompatibility due to het genes is strictly vegetative;
fertility of crosses is not reduced when
parent strains are vegetatively incompatible. Vegetative incompatibility may be manifested in
several
ways: (a) Failure to form stable heterokaryons (715, 889), best seen using complementing auxotrophic or
other forcing markers. (b) Cell death following the fusion of unlike hyphae (721) or after the
microinjection of cytoplasm or extracts into unlike strains (2226). The hyphal segments involved are
sealed off and die; incompatible nuclei do not migrate through septal pores into adjoining cells.
Microinjection implicates proteins in the killing reaction (2213, 2226). (c) Abnormal growth,
morphology, pigmentation, and cell death in colonies of meiotically generated partial diploids
that are
heterozygous for one or more het genes (1421, 1475, 1560) (Fig. 36). Duplication-generating
chromosome rearrangements enable individual het genes to be identified, mapped, and
characterized one
at a time in an otherwise haploid background using the abnormality of heterozygous duplication
progeny
as a criterion (1560, 1578). Cloning of het genes has also made use of the
abnormality of heterozygous
transformants (1346, 1934). (d) Occurrence of a barrage reaction following the
confrontation of
vegetatively incompatible strains (776, 780, 1597). When the interacting strains are of opposite mating
type, het incompatibility is manifested by the appearance of two rows of perithecia
separated by a clear
zone within which killing occurs (Fig. 37). The barrage is seen most clearly when strains are
used that do
not form macroconidia.

het-c, -d, -e, and -i were detected in laboratory strains, using heterokaryon
tests (715, 1630, 2225).
Discovery of het-5 through het-10 was based on the abnormality of duplication
progeny when a series of
duplication-generating rearrangements were crossed with strains from nature (1421). het genes are
polymorphic in natural populations of Neurospora crassa (1425). The mating-type idiomorphs A and a
also act as het genes in N. crassa (134, 721, 1475, 1629). The mat A/mat a vegetative incompatibility
reaction depends on the presence of a functional tol+allele (977, 1466). Genetic differences at other loci
can affect the vigor, stability, and speed of formation of heterokaryons (51, 488, 980). Dominant
suppressors of the incompatibility reaction have been reported that affect one or more het
loci (51).
Rockefeller-Lindegren (RL) wild types are het-C, het-D, het-E (2225), and het-I (2222). St. Lawrence
74A and Oak Ridge (OR) wild types are het-C, het-d, het-e (2225), and het-i (1630, 2222). By definition,
OR strains are hetOR for het loci other than these four (1421), e.g., het-5OR. Tester strains are available
for
identifying and scoring the known het genes (700, 1588). The Wilson-Garnjobst testers for het-c, -d, and
-e are complicated by differences at another locus or loci affecting heterokaryon formation
(980, 2223).
For map locations of het genes and the rearrangements used for testing, see Fig. 1 in ref.
(1588). The
inactive-mating-type helper strain am1ad-3B cyh-1 (779) is useful for determining whether a strain is
het-compatible with OR strains (1564). het gene differences affect the transmission of
mitochondrial
plasmids between strains, both vegetatively (509) and in sexual interactions (508). Vegetative
incompatibility is reviewed in refs. (742), (1176), and (1568).

FIGURE 37 Barrage formation as a manifestation of vegetative (heterokaryon)
incompatibility. Strains of opposite mating
type, mat A and mat a, were inoculated to crossing medium in alternate quadrants of the petri
dish at the positions marked.
When unlike strains come together, a clear zone of inhibition is formed and lines of perithecia
develop on each side of this barrage.
Each strain acts as the maternal parent of perithecia on its own side of the barrage, and the strain
on the opposite side acts as
the fertilizing parent. This is shown in the plate to the right, where the mat a parent carried per
allele PBJ1.
The perithecial color mutant blocks formation of black pigment in the maternally generated
perithecial wall.
The nonblack perithecia, which become orange as carotenoids develop, were fully as numerous
as the black perithecia opposite them
(1569 ).
Parents in these tests all carried a mutant fluffy allele, which improves visibility by eliminating
macroconidia.
Photographs from D. D. Perkins.

Specifies a polypeptide that contains a hydrophobic sequence, a leucine-rich domain, and
a glycine-rich
domain. Allele specificity is due to a highly variable domain of about 40 amino acid residues (1797).
Stable heterokaryons are not formed by strains with het-c alleles that differ in specificity
(715, 716).
Heterozygous duplications show inhibited “brown flat” morphology, spreading to
cover a slant but not
conidiating (1552, 1560) (Figs. 36 and 37). Two alleles found in laboratory strains were
originally called
het-C and het-c (715). Following the discovery and demonstration of a third allele,
het-cPA, the symbol
het-C was changed to het-cOR and the symbol het-c was
changed to het-cEM (1797). Three specificity
types have been recognized and shown to be polymorphic in nature. These are designated
het-cOR, het-cGR, and het-cPA.
(het-cEM is functionally identical to het-cGR.)
Polymorphisms in other Neurospora
species suggest that the known het-c alleles originated prior to divergence of the species
(1797).
Differences at het-c are more effective than those at het-d, het-e, or mat in
preventing the transmission of
mitochondrial plasmids between strains with different allele specificity (509). Called c.

IIR.
Right of fl (25%) (715). Included in duplications from T(ALS176) (1562) and T(OY337) (1578).

Stable
heterokaryons are not formed by strains het-D + het-d (715, 716); het-D/het-d duplications show
inhibited spreading growth on slants, with fine subsurface hyphae and no conidia. These are
distinguishable from het-C/het-c duplications, which have coarser texture (1562).

VIIL.
Between cya-8, T(ALS179) and nic-3 (28%) (1578, 2225). Included in duplications from
T(T54M50).

The
killing reaction following the fusion of het-E and het-e mycelia is more rapid and
severe, and growth
inhibition in het-E/het-e duplication strains is more severe than for the vegetative
incompatibility
mediated by different alleles at het-c or mat (1560, 2225) (Fig. 36).

I or II.
Linked to T(IR;IIR)4637al-1 (1630). Second-division segregation in five of eight asci (2223).

Recognized by cessation of growth of forced heterokaryons. In heterokaryons between the
strains used
by Pittenger (1630), het-i nuclei were eliminated and het-I nuclei
were retained if the initial frequency of
het-I exceeded 30%. When more than 70% of nuclei were het-i, growth
continued without a change of
ratio. In heterokaryons between the RL strains used by Calligan and Wilson, nuclei called
Hi are
eliminated from HI + hi heterokaryons regardless of the starting ratio (2223). The genes Hi and hi
(“heterokaryon instability”) from RL strains are believed to be alleles of
het-I and het-i, which initially
were called I and i.

Vegetative incompatibility, initially recognized by inhibited duplications, was confirmed
using
heterokaryon tests (1421, 1425). Can be scored in duplication progeny from crosses that are
heterozygous for either T(MD2) or T(NM103) (1588).

Duplications heterozygous for het-6 are severely inhibited. Escape from inhibition
occurs by deletion of
a segment carrying one of the het alleles from the partial diploid produced by
T(AR18) (1938).
Vegetative incompatibility was recognized by the production of inhibited duplication progeny
when
strains from nature were crossed by T(AR18), T(P2869), or T(NM149)
(1421, 1578). Confirmed byheterokaryon tests (978). Alleles at het-6 and un-24 are in linkage
disequilibrium, with no coupling-phase recombinant in strains from natural populations (1351).

Vegetative incompatibility initially was recognized by the production of inhibited
duplications from
crosses of wild strains by T(T39M777) (Fig. 36) and was confirmed using heterokaryon
tests (1425).
Crosses of T(T39M777) with isolates from nature indicate that there are either three
alleles (het-8OR, het-8HO, and het-8PA)
or another polymorphic het locus closely linked to het-8 (924).

VIR.
Between T(AR209) and T(OY329)L; hence, between
Cen-VI and trp-2 (1578).

Vegetative incompatibility was recognized by the production of inhibited duplications
from crosses of
wild strains by T(AR209). No heterokaryon test. Photograph of heterozygous
duplication colony (1421).

Identified by the slow growth of transformants obtained using a linkage group V cosmid.
Thought at first
to be a suppressor of het-c-mediated vegetativeincompatibility and then
reinterpreted as containing an
independent functional het gene (1492, 1493). Published information is insufficient to establish the
validity of the postulated het-12 locus.

The
biosynthetic pathway is shown in Fig. 38. Most histidine auxotrophs are inhibited by complex
media
or by certain combinations of amino acids with which histidine does not effectively compete for
permeases of the basic, neutral, and general amino acid transport systems; see Fig. 47. A
histidine mutant
can grow on minimal medium plus histidine in the presence of either a basic amino acid or a
competing
neutral amino acid, but not in the presence of both (809, 1243, 1291). Histidine mutants were not
obtained in early mutant hunts where complex media were used, but were recovered on
histidine-supplemented minimal medium (809, 1159). General studies (329, 809, 2196). Enzymes of
histidine biosynthesis are derepressed coordinately with those of tryptophan, arginine, lysine (292), and
other amino acids [reviewed in ref. (1768)]. See cpc-1. Called hist.

Requires histidine. Blocked prior to IGP (329, 2196), presumably in either EC 5.3.1.16 or EC 2.4.2.-,
which catalyze the only two steps not definitively genetically characterized (Fig. 38). No
intralocus
complementation (95 alleles) (329). Intralocus recombination (314). Used in the first cloning of a
Neurospora telomere (1809).

Many
mutagen-sensitive mutants are also sensitive to inhibition by histidine (see mus, uvs, mei,
and Table
3) (946, 1467, 1830). Certain strains that were first identified as mutant on the basis
of histidine
sensitivity are not sensitive to the few mutagens tested [see, for example, ref. (520) and hss-1]. The
mechanism underlying histidine sensitivity is not understood.

Enables
a his-3 allele to use L-histidinol. Proposed to be due to increased uptake through basic
L-amino
acid transport system III [as defined in ref. (1522)]. The hlp-1 mutation confers increased sensitivity of
lys and arg mutants to inhibition by arginine and lysine, respectively (879).

IR.
Between Tp(T54M94)R, arg-6 (1%) and al-1 (<1%),
al-2 (2%; 7%), cnr (1%). Between breakpoints
of T(STL76) and T(4637); hence, left of al-1 (1548, 1578, 1585). Located on a common cosmid with al-1
(1816).

Neurospracrassa is sensitive to growth inhibition by hygromycin B. The
bacterial gene hph encodes a
phosphotransferase that confers resistance to the fungus (1977), where it has had numerous applications.
The hph gene has been incorporated into cosmid vectors as a selectable marker for use in
transformation
(1502, 1504). Selection for hph expression has been used to obtain
site-specific integration events (277).
hph has been used to study gene silencing (955, 1529). As a reporter, hph has been used to obtain both
cis- and trans-acting mutations that affect gene regulation by asking for increased
hph expression when
expression is normally repressed (677, 1241). Hygromycin phosphotransferase enzyme activity can be
measured in N. crassa extracts (677, 678).

Selected as a suppressor of the double mutant pho-4; pho-5, which lacks both of
the two high-affinity
permeases and is unable to grow at low phosphate concentration and high pH. On ordinary
Vogel’s (high
phosphate) medium, the triple mutant hpp; pho-4; pho-5 accumulates brownish pigment
and does not
grow as well as the pho-4; pho-5 double mutant (1327).

Encodes a 30-kDa heat-shock protein. Mutant obtained by RIP shows reduced viability at
high
temperature and altered location of a 22-kDa protein in mitochondria (1637). Lacks a small a-crystallin-related
heat-shock protein, shows poor survival during heat shock on a nutrient medium with restricted
glucose, and accumulates unphosphorylated glucose at high temperature. Hexokinase is reduced
by more
than 35% in the mutant relative to wild type. HSP30+ may protect hexokinase from
thermal inactivation
(1635).

Encodes a major stress-inducible 70-kDa heat-shock protein (1026), which reaches its highest level in late
aerial hyphae (811). Homolog of Escherichia colidnaK. A molecular
chaperone involved in the
translocation motor for the import of proteins through the mitochondrial membrane into the
matrix (2300)
(Fig. 64). Called hsps, hsps-1. For another member of the hsp70 family,
see grp78.

Encodes an abundant 19-kDa protein of unknown function. Mutants generated by RIP
show lysis of
hyphal tips when grown on solid medium. Patches of bright orange-red pigment are
accumulated.
Hyphal tips below the agar surface produce large balloons or lens-shaped structures. Growth on
high
concentrations of NaCl is indistinguishable from that of wild type (204). Called vac-5 (1447).